One biological explanation of schizophrenia is genetic vulnerability. Studies have shown schizophrenia is more common among family members of sufferers than others in the general population.
About 1% of the population has schizophrenia, and the chance of developing the illness increases to 10% in first degree relatives (such as parents, children and siblings), and the prevalence rate is higher for first degree relatives compared to second degree relatives (uncles, aunts, half siblings etc.) with 10% and 3% prevalence rates respectively, showing there is a link between schizophrenia and genetics.
Genetic vulnerability to mental illness can be supported by physical illnesses (e.g. heart disease, diabetes etc.) having a genetic basis, so some mental illnesses could also be linked to this, however just because schizophrenia is more common amongst relatives of sufferers doesn’t necessarily mean it is due to genetics, as families are usually exposed to the same/similar environmental influences.
Showed that if one identical twin is affected by schizophrenia, there is a 40-60% chance their twin will suffer too. This reduces to 17% in non-identical twins.
Calculated that the pooled data for all schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% compared to only 7.4% for DZ twins, showing a genetic influence.
Kety et al (1988)
In Denmark 33 people from a sample of 5,500 adults who had been adopted were schizophrenic. They were compared with matched controls who didn’t have the disorder. The parents and siblings of these 66 participants (both adoptive and biological) were assessed and diagnosed by a psychiatrist, who didn’t know whether the interviewees were relatives of schizophrenics or not. Around 10% of the relatives were diagnosed with the disorder, and most of these were relatives of the affected adoptees. Almost 14% of these were the biological relatives of the schizophrenic adoptees whereas only 2.7% of the adoptive relatives were diagnosed, supporting the genetic explanation.
The dopamine hypothesis is another biological explanation for schizophrenia, and it suggests people with the disorder have too much dopamine (DA) in the synapses of the brain or are too sensitive to it.
Antipsychotic drugs treat the symptoms of schizophrenia, but have been known to produce side-effects similar to sufferers of Parkinson’s disease, believed to be caused by a lack of dopamine – opposite to schizophrenia and supporting the idea that dopamine is a factor causing the mental illness.
Some patients with Parkinson’s disease have developed psychotic symptoms if they have been given too much L dopa – a treatment for a lack of dopamine, supporting the theory of the dopamine hypothesis.
Depatie and Lal (2001)
Found that Andomorphine, which is a drug which increases the effects of dopamine does not lead to schizophrenic symptoms when given to non-schizophrenic controls. Even if dopamine levels were a causative factor, it may be indirect and must be triggered through an experience such as in a diathesis-stress causation (e.g. abnormal family circumstances giving rise to high levels triggering symptoms – Lloyd et al).
Naheed and Green (2007)
in a review article noted that the atypical anti-psychotic clozapine works by binding to serotonin receptors as well as dopamine receptors and it is said to be the most effective drug treatment for ‘treatment-resistant schizophrenia’ leading to significant improvements in both positive and negative psychotic symptoms, quality of life, social functioning and suicidality.
Dopamine Evaluation/ Serotnon Argument
(+) Schizophrenics show unusually high levels of Homovanillic acid (a waste product of dopamine, which supports this theory as it shows a link between the neurotransmitter and the disorder.
(-) The dopamine hypothesis cannot be a complete explanation as antipsychotics block D2 receptors very quickly, but symptoms take weeks to reduce, suggesting other factors are involved. As well as this, there is the issue of an indefinable cause and effect with this explanation, as schizophrenia may be caused due to faulty chemicals in the body, or it may be that the body changes and develops chemical faults due to schizophrenia.
Furthermore studies have shown that typical (older) antipsychotics which blocked DA and reduced positive (type 1) symptoms such as hallucinations, yet they were ineffective on Type 2 (negative) symptoms.
Therefore dopamine cannot be proven as the single cause of SZ. A type (modern) antipsychotics work both on dopamine and serotonin levels.
These new anti-psychotics are able to treat both positive and negative symptoms, serotonin was used in anti-depressants before this and since they type 2 symptoms of schizophrenia share many characteristics with the symptoms of depression, therefore by joining the two neurotransmitters together the anti-psychotics can now treat both types of schizophrenias symptoms.
The psychodynamic approach views schizophrenia as the result of the disintegration of the ego.
According to Neo-Freudians, some types of abnormal upbringing – particularly if there is a cold, rejecting ‘schizogenic’ mother – can result in a weak and fragile ego, whose ability to contain the Id’s desires is limited.
This can lead to the ego being ‘broken apart’ by its attempt to control the Id, leaving the Id in overall control. If the ego then loses control, then the person will lose contact with reality.
They will no longer be able to distinguish between themselves and others, their desires and reality as an ego is required to connect with reality. The individual therefore regresses to a state of ‘primary narcissism , much like an infant at the oral stage of psychosexual development who has not yet developed an ego or superego, who’s Id’s pleasure seeking drives their actions.
Dominated by their animal instincts, incapable or organising their own behaviour and hallucinating as a result of their basic inability to distinguish between their imaginations and reality.
Found that schizophrenics reported a higher recall of double-bind statements by their mothers than non-schizophrenics. This supports the idea of a ‘schizogenic mother’ causing schizophrenia by causing a disturbed and confusing upbringing
Hogarty et al (1991)
Found that therapy which reduced over expressed emotion in the families of schizophrenics also reduced the relapse rate. This supports the idea that if a family has controlled the schizophrenics life and emotional atmosphere, to the point of stifling any development of an ego, then after therapy, once the schizophrenic individual has had the time and space to develop a functioning ego, then their Id led schizophrenic episodes would disappear and be controlled by this newly evolved ego.
(-) Berger’s research rests on the self-report and recall of schizophrenics, who may be suffering from paranoia, which may affect their objective recollection of their mothers behaviour earlier in life. Therefore any conclusion of a difference in parenting by the mother inducing schizophrenia within her children is unfounded being supported purely by unreliable research.
(-)Additionally overall the psychodynamic view is not highly regarded anymore. With the development of effective anti-psychotic drugs in the 1950’s and 60’s, the biological view became much more largely regarded over the psychological theories which have never really recovered.